MARINE TOXINS AND VENOMOUS AND POISONOUS MARINE ANIMALS
343
small amounts of the venom are injected is bradycardia with an increase
in the PR interval giving a first, second or third degree atrioventricular
block. The second degree block is usually followed by sinus arrest.
Reversal of the small dose effect occurs within 30 sec following the end
of the injection. Cats receiving larger amounts of the venom show,
in addition to the PR interval change, almost immediate ST, T wave
change indicative of ischemia and, in some animals, true muscle injury.
High concentrations cause marked vasoconstriction of the large arteries
and veins as well as the arterioles. Much more serious is the direct
effect on the heart muscle. The venom produces changes in heart rate
and amplitude of systole, and may cause complete, often irreversible,
cardiac standstill. It is apparent that the venom affects the normal
pacemaker. The new rhythm evoked following cardiac standstill is
often irregular and appears to be elaborated outside the sino-atrial node
(Russell and van Harreveld, 1954 ; Russell et al., 1957).
While part of this depression
is secondary to the cardiovascular changes, the venom may have
a direct effect on the respiratory centers of the medulla. The toxin
produces many changes in the behaviour of animals. Some of these
changes can be attributed to the direct effects of the venom on the
central nervous system. I n mammals the venom occasionally produces
convulsive seizures. The mechanism of these seizures is not clear.
They may be due in part to cardiovascular failure. Seizure patterns
were not seen in electroencephalograms from anesthetized animals
(Russell et al., 1958a).
The venom does not appear to have a deleterious effect on neuromuscular transmission (Russell and Long, 1960 ; Russell and Bohr,
1962). When injected into the lateral ventricles of mammals it, produced some slight apathy, astasia and licking motions, all of which
were transient (Russell and Bohr, 1962). The LD,, has been calculated
as 28.0 mg dried crude venom per kg mice (Russell et al., 1958b).
Mice injected with a lethal dose of U. halleri venom develop hyperkinesis, prostration, marked dyspnea, blanching of the ears and
retina, and exophthalmos. These are followed by complete atonia,
gasping respiratory movements, coma and death. In cats the same
syndrome is seen. Ataxia, dilated pupils, increased salivation, micturation, defecation, marked atonia, cyanosis and hypoactive or absent
deep and superficial reflexes are also found. I n monkeys a similar
pattern is observed. I n one monkey we observed a tonic-clonic
generalized motor seizure accompanied by increased salivation,
twitching of the head and marked dilation of the pupils (Russell
et al., 1958a).
The venom depresses respiration.
343
small amounts of the venom are injected is bradycardia with an increase
in the PR interval giving a first, second or third degree atrioventricular
block. The second degree block is usually followed by sinus arrest.
Reversal of the small dose effect occurs within 30 sec following the end
of the injection. Cats receiving larger amounts of the venom show,
in addition to the PR interval change, almost immediate ST, T wave
change indicative of ischemia and, in some animals, true muscle injury.
High concentrations cause marked vasoconstriction of the large arteries
and veins as well as the arterioles. Much more serious is the direct
effect on the heart muscle. The venom produces changes in heart rate
and amplitude of systole, and may cause complete, often irreversible,
cardiac standstill. It is apparent that the venom affects the normal
pacemaker. The new rhythm evoked following cardiac standstill is
often irregular and appears to be elaborated outside the sino-atrial node
(Russell and van Harreveld, 1954 ; Russell et al., 1957).
While part of this depression
is secondary to the cardiovascular changes, the venom may have
a direct effect on the respiratory centers of the medulla. The toxin
produces many changes in the behaviour of animals. Some of these
changes can be attributed to the direct effects of the venom on the
central nervous system. I n mammals the venom occasionally produces
convulsive seizures. The mechanism of these seizures is not clear.
They may be due in part to cardiovascular failure. Seizure patterns
were not seen in electroencephalograms from anesthetized animals
(Russell et al., 1958a).
The venom does not appear to have a deleterious effect on neuromuscular transmission (Russell and Long, 1960 ; Russell and Bohr,
1962). When injected into the lateral ventricles of mammals it, produced some slight apathy, astasia and licking motions, all of which
were transient (Russell and Bohr, 1962). The LD,, has been calculated
as 28.0 mg dried crude venom per kg mice (Russell et al., 1958b).
Mice injected with a lethal dose of U. halleri venom develop hyperkinesis, prostration, marked dyspnea, blanching of the ears and
retina, and exophthalmos. These are followed by complete atonia,
gasping respiratory movements, coma and death. In cats the same
syndrome is seen. Ataxia, dilated pupils, increased salivation, micturation, defecation, marked atonia, cyanosis and hypoactive or absent
deep and superficial reflexes are also found. I n monkeys a similar
pattern is observed. I n one monkey we observed a tonic-clonic
generalized motor seizure accompanied by increased salivation,
twitching of the head and marked dilation of the pupils (Russell
et al., 1958a).
The venom depresses respiration.